Pathoma--Chapter 1-High Yield

Question 1

t(15,17)

1. causes what disease
2. what gene is involved
3. what is the treatment

Answer 1

1. acute promyelocytic leukemia
2. trans-retinoic acid receptor
   - disrupts vitamin a receptor–cells are trapped in blast state
3. tx: ATRA-all transretionic acid
   - ability to bind to receptors and allow for maturation of neutrophils

Question 2

what type of metaplasia does not increase risk of malignancy?

Answer 2

apocrine metaplasia

Question 3

what is the cell type that lines the esophagus?

Answer 3

squamous epithelium

Question 4

what cell type is seen in barretts esophagus?

Answer 4

mucinous nonciliated columnar epithelium–able to withstand acidic environment

Question 5

what are the 3 permanent cell types in the body?

Answer 5

1. cardiac myocytes
2. skeletal muscle
3. nerves

Question 6

what is the difference between hypertrophy and hyperplasia?

Answer 6

hypertrophy– increase in cell size
(the 3 permanent cell types in body can only undergo hypertrophy)
hyperplasia–increase in # of cells

Question 7

what are the two processes that facilitate atrophy of a cell?

Answer 7

1. Ubquitin proteasome pathway–proteins (cytoskeleton) are marked and then degraded
2. autophagy- vesicular degradation

Question 8

vitamin A deficiency can result in what three things?

Answer 8

1. night blindness
2. proper maturation of cells of immune cell
3. maintence of squamous epithelium (conjuctiva)

Question 9

deficiency in vitamin A can cause what to occur in the eyes?

Answer 9

keratomalacia

-vitamin a def–> metaplasia of cells–> thickening of conjuctiva

Question 10

what is myositis ossificans?

Answer 10

• metaplasia of the mesenchymal cells (connective tissue)

- conversion of skeleton muscle to bone

Question 11

dysplasia arises 2/2 to

Answer 11

• pathologic hyperplasia or metaplasia
  ex) endometrial hyperplasia–> dysplasia–>endometrial carcinoma
  ex) baretts esopagus

Question 12

is dysplasia reversible?

Answer 12

YES!!

but if persists–> carcinoma (non-reversible)

Question 13

what is an example of agenesis?

Answer 13

renal agenesis

Question 14

what is an example of hypoplasia?

Answer 14

streak ovary in Turners syndrome

Question 15

what are the enzymes that are critical in activating apoptosis?

Answer 15

caspases

Question 16

what is the role of bcl2 and cytochrome c in mediating cell death?

Answer 16

1. bcl2 stablizes the mitochondrial membrane

2. when bcl2 is lost, cytochrome c is able to leave the mitochondria–> activate caspases–> apoptosis

Question 17

what cell utilizes the fast-death receptor pathway to mediate cell death?

Answer 17

T cell (CD98)--> negative selection in the thymus
-avoid autoimmune activation

Question 18

how do Tc cells kill other cells?

Answer 18

apoptosis
-recognize, release perforins to make pores in the membrane, granzyme will enter the pores and activate caspases–> apoptosis

Question 19

where is the electron transport chain located?

Answer 19

inner mitochondrial membrane

Question 20

what is the most damaging free radical?

Answer 20

hydroxyl

Question 21

during the electron transport chain, oxygen accepts _____ electrons–> H20.

Answer 21

4 electrons

Question 22

what is produced if oxygen fails to recieve all 4 electrons

Answer 22

O2–> O2–> H2O2–> OH–> H20

production of free radicals (O2, H202, OH)

Question 23

what two metals can pathologically produce free radicals?

Answer 23

copper & iron
(both are tightly bound when in body)

iron produces free radicals thru the fentin rxn

*hemachromatosis & wilsons disease (excessive iron and copper respectively)–>tissue damage 2/2 to excess of free radicals

Question 24

how do free radicals lead to dna damage?

Answer 24

oxidation

Question 25

what enzymes play a role in removing the three different free radicals?

Answer 25

1. O2* (superoxide)–> superoxide dismutase
2. H202(hydrogen peroxide)–> catalase
3. OH* (hydroxyl free radical)–> glutathione peroxidase

Question 26

what is the free radical that is concerning for people in the dry cleaning industry?

Answer 26

CCl4–> CCl3* radical

• converted in hepatocytes via cytoP450
• lead to reversible hepatic injury (cell swelling–> swelling of RER and popping off of the ribosomes–> decrease in protein synthesis)
• -> reduction in apopliproteins & the fat that is entering the liver to be reconsolidated remains in the liver
• pathologic findings: hepatic steatosis